Heart failure is a complex clinical syndrome that results from any functional or structural heart disorder, impairing ventricular filling or ejection of blood to the systemic circulation to meet the systemic needs. Heart failure can be caused by diseases of the endocardium, myocardium, pericardium, heart valves, vessels or metabolic disorders. Most patients with Heart failure have symptoms due to impaired left ventricular myocardial function. Patients usually present with symptoms of dyspnea, decreased exercise tolerance and fluid retention, characterized by pulmonary and peripheral edema.
Heart failure due to left ventricular dysfunction is categorized according to left ventricular ejection fraction (LVEF) into heart failure with reduced ejection fraction (usually considered LVEF 40% or less), known as HFrEF and heart failure with preserved ejection fraction; known as HFpEF. The definition of HFrEF has varied among different studies and guidelines with different left ventricular ejection fraction (LVEF) cut-offs of ≤35%, <40%, and ≤40%. Randomized controlled trials in patients with HF have mainly enrolled patients with HFrEF with an EF ≤35% or ≤40%, and it is only in these patients that efficacious therapies have been demonstrated to date. According to the most recent ACC/AHA guidelines on heart failure, HFrEF is defined as the clinical diagnosis of HF with EF ≤40%. In routine clinical practice, many clinicians would consider EF <45% as significant systolic dysfunction and would consider it as HFrEF.
Heart failure with preserved ejection fraction (HFpEF) on the other hand has also been variably classified as EF >40%, >45%, >50%, and/or ≥55%. The term HFpEF has been used since some of these patients do not have entirely normal EF but also do not have a major reduction in the systolic function. Patients with an EF between the range of 40% to 50% have been considered to represent an intermediate group of patients due to a variable cut off used for systolic dysfunction by the different studies. These patients should be routinely treated for underlying risk factors and comorbidities and with optimal guideline-directed therapy, similar to that of HFrEF.
When heart failure develops, compensatory mechanisms attempt to increase the cardiac filling pressure, muscle mass and heart rate. However, in many cases, there is usually a progressive decline in heart function.
Heart failure is caused by several disorders, including diseases affecting the pericardium, myocardium, endocardium, cardiac valves, vasculature, or metabolism.
The most common causes of systolic dysfunction (HFrEF) are idiopathic dilated cardiomyopathy (DCM), coronary heart disease (ischemic), hypertension, and valvular disease.
Hypertension, obesity, coronary artery disease, diabetes mellitus, atrial fibrillation, and hyperlipidemia are highly prevalent in HFpEF patients. Hypertension by far is the most important cause of HFpEF. In addition, conditions like hypertrophic obstructive cardiomyopathy, and restrictive cardiomyopathy are associated with significant diastolic dysfunction, leading to HFpEF.
Causes of high-output failure include:
Very common causes of decompensation in a stable patient with HF include:
Approximately 5.1 million people in the United States have clinically manifest heart failure, and the prevalence continues to increase. Heart failure incidence has remained stable over the past decades, with more than 650,000 new cases of heart failure cases diagnosed annually, especially for individuals greater than 65 years of age. Because prevalence is greater in this age group, heart failure prevalence is expected to worsen in the near future.Epidemiological differences have been noted. Black men have the highest incidence rate (1000 person-years) for heart failure and the greatest five-year mortality rate when compared to whites. White women represent the lowest incidence. Heart failure in non-Hispanic black males and females has a prevalence of 4.5% and 3.8%, respectively, versus 2.7% and 1.8% in non-Hispanic white males and females, respectively. Although survival has improved, the absolute mortality rates for patients with heart failure remain approximately 50% within five years of diagnosis. The survival rate is inverse proportional to the staging severity of heart failure. The 5-year survival for stage A, B, C, and D heart failure was found to be 97%, 96%, 75%, and 20%, respectively in a study.
By 2013, heart failure costs in the United States exceeded $30 billion.
Gender differences in heart failure:
Heart failure in Developing nations
The adaptive mechanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac performance. The primary myocardial response to chronically increased wall stress is myocyte hypertrophy, death due to apoptosis, and regeneration. This process eventually leads to remodeling, usually the eccentric type, and reduced cardiac output, causing a cascade of the neurohumoral and vascular mechanism.
Decreased carotid baroreceptor stimulation and renal perfusion will activate the sympathetic nervous system and Renin-Angiotensin-Aldosterone system.
Sympathetic nervous system activation will cause increased heart rate and inotropy, leading to myocardial toxicity. Renin-Angiotensin-Aldosterone system activation leads to vasoconstriction, increasing afterload (angiotensin II) and hemodynamic alterations, increasing preload (aldosterone).
Both BNP and ANP are peptides released from the atria and ventricles in reposne to heart chamber pressure/volume expansion. These peptides promote natriuresis and vasodilatation. In addition. BNP inhibits the reabsorption of sodium in the proximal convoluted tubule. It also suppresses renin and aldosterone release.
In patients with HFpEF there is impaired relaxation and increasing ventricle stiffness, leading to dysfunction in diastolic filling of the left ventricle. Patients with concentrcleft ventricular hypertrophy have a shift of the diastolic pressure volume curve to the left, leading to elevation in diastolic pressures, which leads to increased energy expenditure and oxygen demand and myocardial ischemia.
All of these mechanisms will cause negative remodeling and worsen the left ventricular function, causing symptoms of heart failure.
Symptoms of heart failure include those due to excess fluid accumulation (dyspnea, orthopnea, edema, pain from hepatic congestion, and abdominal distention from ascites) and those due to a reduction in cardiac output (fatigue, weakness) that is most pronounced with physical exertion.
Acute and subacute presentations (days to weeks) are characterized by shortness of breath at rest and/or with exertion, orthopnea, paroxysmal nocturnal dyspnea, and right upper quadrant discomfort due to acute hepatic congestion (right heart failure). Palpitations, with or without lightheadedness can occur if patient develops atrial or ventricular tachyarrhythmias
Chronic presentations (months) differ in that fatigue, anorexia, abdominal distension, and peripheral edema may be more pronounced than dyspnea. The anorexia is secondary to several factors including a poor perfusion of the splanchnic circulation, bowel edema, and nausea induced by hepatic congestion.
Diuretics, beta-blockers, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, angiotensin receptor neprilysin inhibitor, hydralazine plus nitrate, digoxin, and aldosterone antagonists can produce an improvement in symptoms
Prolongation of patient survival has been documented with beta blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor neprilysin inhibitor, hydralazine plus nitrate, and aldosterone antagonists. More limited evidence of survival benefit is available for diuretic therapy. Replace an angiotensin converting enzyme inhibitors or angiotensin receptor blockers by angiotensin receptor neprilysin inhibitor in chronic symptomatic patients with CHF NYHA class II-III with an adequate blood pressure who are tolerating an optimal dose of these medications. Angiotensin receptor neprilysin inhibitor should not be given within 36 hrs of angiotensin converting enzyme inhibitors dose.
In African-Americans, hydralazine plus oral nitrate is indicated in patients with persistent NYHA class III to IV HF and LVEF less than 40%, despite optimal medical therapy (beta-blocker, angiotensin converting enzyme inhibitors, ARB, aldosterone antagonist (if indicated), and diuretics.
Device therapy: implantable cardioverter-defibrillator (ICD) is used for primary or secondary prevention of sudden cardiac death. Cardiac resynchronization therapy with biventricular pacing can improve symptoms and survival in selected patients who are in sinus rhythm and have a reduced left ventricular ejection fraction and a prolonged QRS duration. Most patients who satisfy criteria for cardiac resynchronization therapy implantation are also candidates for an implantable cardioverter-defibrillator and receive a combined device.
A ventricular assist device (bridge to transplant or as a destination therapy) or cardiac transplant are reserved for those with severe disease despite all other measures.
NYHA Classification of Heart failure
ACC Heart Failure Stages:
Heart failure is a serious medical disorder associated with high mortality. Mortality rates at 1 year and 5 years are 22% and 43%, respectively. The highest mortality is in patients with advanced NYHA class. In addition, heart failure associated with an MI carries a mortality of 30-40%. Heart failure that is associated with systolic dysfunction has a 50% mortality over 5 years. Further, patients with heart failure need repeated admissions over the years.
To reduce heart failure hospitalizations, it is reasonable (class IIa) to use Ivabradine in patients with NYHA II-III with guideline-directed medical therapy (including a beta-blocker) and heart rate of more than 70 bpm.
Heart failure disease management is a complex condition that requires a multidisciplinary framework for the care of patients, including discharge planning, patient education, and frequent outpatient assessment.
Heart failure is a serious disorder that is best managed by an interprofessional team that includes the primary care physician, emergency department physician, cardiologist, radiologist, cardiac nurses, internist, and a cardiac surgeon. It is imperative to treat the primary cause of heart failure. Healthcare workers including nurses who look after these patients must be familiar with current guidelines on treatment. The risk factors for heart disease must be modified and the pharmacist should educate the patient on the importance of medication compliance. The dietitian should educate the patient on the importance of a low salt diet and limiting fluid intake. The nurse should educate the patient on the importance of exercise, avoiding stress and ensuring follow up with the cardiologist. The pharmacist should ensure that the patient understands the importance of medication compliance, which is often the single most important factor leading to decompensation. Patients need to be educated on the importance of maintaining a healthy body weight, discontinuation of smoking, controlling blood pressure and ensuring normoglycemia. A cardiac nurse should follow these patients and monitor their progress. The only way to lower morbidity and mortality is through open communication between the team members.
When the condition is not managed appropriately, it is associated with high morbidity and mortality, including a poor quality of life.